美國研究人員6月12日在英國《自然—遺傳學》雜志網絡版上發(fā)表研究報告稱,，偏頭痛與3個基因變異有關,。這一發(fā)現有助于了解偏頭痛的發(fā)病機制，并為以該基因為靶向開發(fā)治療藥物奠定基礎,。
美國布里格姆婦科醫(yī)院的研究人員對超過2.3萬名婦女的基因數據進行了分析，這些婦女中有5000多人患有偏頭痛,。在這份全基因組關聯研究中,，研究人員在約30億個人類基因堿基對中，找出了具有關聯性的序列,。
結果顯示,，偏頭痛患者的3個基因較常出現變異，這3個基因分別為TRPM8,，LRP1和PRDM16,。如果被調查女性的上述基因中的任何一個發(fā)生變異，她們患偏頭痛的幾率會提高10%至15%,。
據研究者介紹,，TRPM8基因控制著人們對寒冷和疼痛的敏感程度,，LRP1基因負責向神經元傳遞信號。PRDM16基因能夠調控肌肉脂肪代謝,，其與偏頭痛的關聯正在研究中,。
雖然偏頭痛發(fā)生的確切原因不明，但普遍觀點認為偏頭痛與遺傳因素有關,。多項醫(yī)學研究顯示,，神經細胞對刺激物的過度反應是導致偏頭痛的重要原因，女性患偏頭痛的幾率是男性的3到4倍,。
研究人員指出,，盡管這一發(fā)現是偏頭痛研究中的一大進展，但不足以就此下結論說偏頭痛是由這3個基因變異造成的,，研究人員仍需對此進行更深入的研究,，以確定造成偏頭痛的真正原因。（生物谷Bioon.com）
生物谷推薦原文出處：
Nature Genetics DOI:10.1038/ng.856
Genome-wide association study reveals three susceptibility loci for common migraine in the general population
Daniel I Chasman; Markus Schürks; Verneri Anttila; Boukje de Vries; Ulf Schminke; Lenore J Launer; Gisela M Terwindt; Arn M J M van den Maagdenberg; Konstanze Fendrich; Henry V?lzke; Florian Ernst; Lyn R Griffiths; Julie E Buring; Mikko Kallela; Tobias Freilinger; Christian Kubisch; Paul M Ridker; Aarno Palotie; Michel D Ferrari; Wolfgang Hoffmann; Robert Y L Zee; Tobias Kurth
Migraine is a common, heterogeneous and heritable neurological disorder. Its pathophysiology is incompletely understood, and its genetic influences at the population level are unknown. In a population-based genome-wide analysis including 5,122 migraineurs and 18,108 non-migraineurs, rs2651899 (1p36.32, PRDM16), rs10166942 (2q37.1, TRPM8) and rs11172113 (12q13.3, LRP1) were among the top seven associations (P < 5 × 10?6) with migraine. These SNPs were significant in a meta-analysis among three replication cohorts and met genome-wide significance in a meta-analysis combining the discovery and replication cohorts (rs2651899, odds ratio (OR) = 1.11, P = 3.8 × 10?9; rs10166942, OR = 0.85, P = 5.5 × 10?12; and rs11172113, OR = 0.90, P = 4.3 × 10?9). The associations at rs2651899 and rs10166942 were specific for migraine compared with non-migraine headache. None of the three SNP associations was preferential for migraine with aura or without aura, nor were any associations specific for migraine features. TRPM8 has been the focus of neuropathic pain models, whereas LRP1 modulates neuronal glutamate signaling, plausibly linking both genes to migraine pathophysiology.
